CFB PBL 5

Question 1

Describe the role of peripheral and central chemoreceptors in the control of breathing

Answer 1

CHEMORECEPTORS: sensory organs, respond to changes in O2 + CO2

Peripheral chemoreceptors: located in carotid + aortic bodies
respond to O2 level changes
low levels O2 signal respiratory centre via cranial nerves 9 and 10, this increases ventilation

Central chemoreceptors: found in medulla oblongata
respond indirecrtly to CO2 via H+
Increased CO2 levels converted to HCO3- and H+
rreceptors detect increase in pH - signals sent to respiratory centre
Increase ventilation

Question 2

State the causes of pulmonary embolism and explain the mechanisms by which they cause it

Answer 2

PREGNANCY:
- growing baby, presses near by veins, causing platelets to adhere to vascular endothelial cells
-

INNACTIVITY: innactivity of skeletal mucle pump releases platelets and clotting factors. These make contact with vascular endothelium which triggers activation of clotting cascade

SURGERY: Damage to endothelial cells. exposes collagen which leads to activation of platelet + clotting factors, leading to activation of clotting cascade

INHERITED: Antithromin III deficiency - this is an anticoagulation factor. Works by binding to thrombin and clotting factors 7, 9, 10, 12. therefore, deficiency leads to clot formation

ORAL CONTRACEPTIVES: Causes hypercoagulation, as increases amount of clotting factor and decreased amount of protein C and antithrimbin III

Question 3

Explain the haemodynamic changes following PE and explain their physiological causes

Answer 3

HAEMODYNAMIC CHANGE: means pressure and vplume changes

a) embolous (clot) impact -> acute increase in right ventricular afterload (because you are pumping against obstruction) -> increase in right atrail pressure -> increases central venous pressure (pressure in vena cava)

b) embolous (clot) impact -> pulmonary hypertenstion -> increased right ventricular pressure -> increase right ventricular blood volume -> stretch + enlargement of RV -> tricuspid valve leaflets (cusps) stretch -> regurgitation into RA during systole -> increase RA blood volume -> increase in jugular vein poressure

(c) Embolous impact -> obstruction of blood flow -> decreased blood return to left side -> decreased EDV -> decreased stroke vol + cardiac output -> decreased BP

Question 4

Describe the clinical features of PE

Answer 4

Clinical features depend on the size of the embolisms

SMALL EMBOLISM:

-impacts terminal arteries and arterioles, unlikely to cause any symptoms
-if small artery is near pleural membranes, leads to inflammation of pleural membranem, which leads to pleural effusion, which leads to pleuritic chest pain

LARGE EMBOLISM

-leads to major arteriole obstruction which leasds to acute pulmonary hypertension, this leads to right side heart failure
-if large embolism breaks up, small clots can travel to distill arteries / arterioles. If these blood vessels located near pleural membrane, this leads to pleural effusion, therefore chest pain

CLINICAL MANIFESTATIONS:

• collapse
  -breathlesness
  -increased JVP
  -pleural effusion
  -crackles
  -pulmonary hypertension
  -low blood pressure
  -right ventricular failure
  -coughing up blood

Question 5

Describe the changes of arterial blood gases after a major pulmonary embolism

Answer 5

LOW OXYGEN LEVELS
-obstruction by clot, impedes gas exchange
-inflammation, leading to oedema in lungs, therefore, fluid in alveoli impedes gas exchange

LOW CO2 LEVELS
-activation of central chemoreceptors, lead to hyperventilation
-these chemoreceptors activated due to initial high CO2 levels

LOW BLOOD SATUATION PO2
-due to low oxygen levels